TY - JOUR
T1 - The link between childhood trauma and depression
T2 - Insights from HPA axis studies in humans
AU - Heim, Christine
AU - Newport, D. Jeffrey
AU - Mletzko, Tanja
AU - Miller, Andrew H.
AU - Nemeroff, Charles B.
N1 - Funding Information:
This work was supported by NIH Grants MH-58922, MH-73698, and RR-00039. Dr. Heim received funding from NARSAD, ADAA, CDC, and the German Science Foundation. The findings and conclusions in this article are those of the authors and do not necessarily represent the views of the funding agencies.
Funding Information:
Andrew H. Miller : Dr. Miller has served as a consultant for Schering-Plough and Centocor, and has received research funding from Janssen/Johnson and Johnson, GlaxoSmithKline, and Schering-Plough.
Funding Information:
Christine Heim : Dr. Heim received research grants from the National Alliance for Research on Schizophrenia and Depression (NARSAD), Anxiety Disorders Association of America (ADAA), Eli Lilly, Novartis, National Institutes of Health (NIH), and Centers for Disease Control & Prevention (CDC).
Funding Information:
This work was supported by NIH Grants MH-58922, MH-73698, and RR-00039. Dr. Heim received funding from NARSAD, ADAA, CDC, and the German Science Foundation.
Funding Information:
D. Jeffrey Newport has received research support from Eli Lilly, Glaxo SmithKline (GSK), Janssen, National Alliance for Research on Schizophrenia and Depression (NARSAD), National Institutes of Health (NIH), and Wyeth. He has served on speakers’ bureaus and/or received honoraria from AstraZeneca, Eli Lilly, GSK, Pfizer and Wyeth.
PY - 2008/7
Y1 - 2008/7
N2 - Childhood trauma is a potent risk factor for developing depression in adulthood, particularly in response to additional stress. We here summarize results from a series of clinical studies suggesting that childhood trauma in humans is associated with sensitization of the neuroendocrine stress response, glucocorticoid resistance, increased central corticotropin-releasing factor (CRF) activity, immune activation, and reduced hippocampal volume, closely paralleling several of the neuroendocrine features of depression. Neuroendocrine changes secondary to early-life stress likely reflect risk to develop depression in response to stress, potentially due to failure of a connected neural circuitry implicated in emotional, neuroendocrine and autonomic control to compensate in response to challenge. However, not all of depression is related to childhood trauma and our results suggest the existence of biologically distinguishable subtypes of depression as a function of childhood trauma that are also responsive to differential treatment. Other risk factors, such as female gender and genetic dispositions, interfere with components of the stress response and further increase vulnerability for depression. Similar associations apply to a spectrum of other psychiatric and medical disorders that frequently coincide with depression and are aggravated by stress. Taken together, this line of evidence demonstrates that psychoneuroendocrine research may ultimately promote optimized clinical care and help prevent the adverse outcomes of childhood trauma.
AB - Childhood trauma is a potent risk factor for developing depression in adulthood, particularly in response to additional stress. We here summarize results from a series of clinical studies suggesting that childhood trauma in humans is associated with sensitization of the neuroendocrine stress response, glucocorticoid resistance, increased central corticotropin-releasing factor (CRF) activity, immune activation, and reduced hippocampal volume, closely paralleling several of the neuroendocrine features of depression. Neuroendocrine changes secondary to early-life stress likely reflect risk to develop depression in response to stress, potentially due to failure of a connected neural circuitry implicated in emotional, neuroendocrine and autonomic control to compensate in response to challenge. However, not all of depression is related to childhood trauma and our results suggest the existence of biologically distinguishable subtypes of depression as a function of childhood trauma that are also responsive to differential treatment. Other risk factors, such as female gender and genetic dispositions, interfere with components of the stress response and further increase vulnerability for depression. Similar associations apply to a spectrum of other psychiatric and medical disorders that frequently coincide with depression and are aggravated by stress. Taken together, this line of evidence demonstrates that psychoneuroendocrine research may ultimately promote optimized clinical care and help prevent the adverse outcomes of childhood trauma.
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U2 - 10.1016/j.psyneuen.2008.03.008
DO - 10.1016/j.psyneuen.2008.03.008
M3 - Article
C2 - 18602762
AN - SCOPUS:46249091103
SN - 0306-4530
VL - 33
SP - 693
EP - 710
JO - Psychoneuroendocrinology
JF - Psychoneuroendocrinology
IS - 6
ER -